The role of transient receptor potential channel blockers in human gastric cancer cell viability

2012 ◽  
Vol 90 (2) ◽  
pp. 175-186 ◽  
Author(s):  
Byung Joo Kim ◽  
Sung-Young Kim ◽  
Sanghoon Lee ◽  
Ju-Hong Jeon ◽  
Hirofumi Matsui ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Growth And Survival ◽  
Lox Inhibitors ◽  
Transient Receptor

Transient receptor potential cation channel, subfamily M, receptor 7 (TRPM7) is a ubiquitous divalent-selective ion channel with its own kinase domain. Human gastric cancer cells express the TRPM7 channel, and the presence of this channel is essential for cell survival. Recent studies have suggested that 5-lipoxygenase (5-LOX) inhibitors are potent blockers of the TRPM7 channels. The aim of this study was to show the effects of 5-LOX inhibitors on the growth and survival of gastric cancer cells. Among 5-LOX inhibitors, nordihydroguaiaretic acid (NDGA), 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (AA861), and 3-[1-(p-chlorobenzyl)-5-(isopropyl)-3-tert-butylthioindol-2-yl]-2,2-dimethylpropanoic acid (MK886) were potent blockers of TRPM7-like currents in gastric cancer cells and also induced cell death. However, zileuton was ineffective in suppressing TRPM7-like current activity and inducing cell death. Moreover, a specific transient receptor potential cation channel, subfamily C, member 3 (TRPC3) inhibitor, a pyrazole compound (Pyr3), and a specific melastatin TRP (TRPM4) inhibitor, 9-phenanthrol, did not affect TRPM7-like currents or induce cell death. We conclude that TRPM7 has an important role in the growth and survival of gastric cancer cells and a likely potential target for the pharmacological treatment of gastric cancer.

scholarly journals Identification of a novel biomarker in tangeretin‑induced cell death in AGS human gastric cancer cells

2018 ◽  
Author(s):  
Silvia Yumnam ◽  
Suchismita Raha ◽  
Seong Kim ◽  
Venu Venkatarame Gowda Saralamma ◽  
Ho Lee ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

scholarly journals Transient Receptor Potential Cation Channels in Cancer Therapy

2019 ◽  
Vol 7 (12) ◽  
pp. 108 ◽  
Author(s):  
Giorgio Santoni ◽  
Federica Maggi ◽  
Maria Beatrice Morelli ◽  
Matteo Santoni ◽  
Oliviero Marinelli
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Cancer Cells ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Chemotherapeutic Agents ◽  
Migration And Invasion ◽  
Transient Receptor

In mammals, the transient receptor potential (TRP) channels family consists of six different families, namely TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPML (mucolipin), TRPP (polycystin), and TRPA (ankyrin), that are strictly connected with cancer cell proliferation, differentiation, cell death, angiogenesis, migration, and invasion. Changes in TRP channels’ expression and function have been found to regulate cell proliferation and resistance or sensitivity of cancer cells to apoptotic-induced cell death, resulting in cancer-promoting effects or resistance to chemotherapy treatments. This review summarizes the data reported so far on the effect of targeting TRP channels in different types of cancer by using multiple TRP-specific agonists, antagonists alone, or in combination with classic chemotherapeutic agents, microRNA specifically targeting the TRP channels, and so forth, and the in vitro and in vivo feasibility evaluated in experimental models and in cancer patients. Considerable efforts have been made to fight cancer cells, and therapies targeting TRP channels seem to be the most promising strategy. However, more in-depth investigations are required to completely understand the role of TRP channels in cancer in order to design new, more specific, and valuable pharmacological tools.

scholarly journals Silencing of acetyl-CoA carboxylase-α gene in human gastric cancer cells inhibits proliferation via induction of apoptosis, autophagy and suppression of cell invasion

2021 ◽  
Vol 18 (10) ◽  
pp. 2025-2030
Author(s):  
Chunsong Yu ◽  
Xuehong Wu ◽  
Bihua Yao ◽  
Huaxing Tao
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Annexin V ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Acetyl Coa Carboxylase ◽  
Gastric Cancer Cells ◽  
Acetyl Coa

Purpose: To study the role and therapeutic potential of acetyl-CoA-carboxylase-α (ACC) in the management of gastric cancer. Methods: Expression of ACC in gastric cancer cell lines was determined using quantitative real-time polymerase chain reaction (qRT-PCR). Lipofectamine 2000 reagent was used for transfection, while cell viability was determined by MTT assay. Apoptotic cell death was assayed with 4′, 6-diamidino-2- phenylindole (DAPI) and acridine orange/ethidium bromide (AO/EB) staining. The proportion of apoptotic cells was estimated with Annexin V/PI staining. Wound healing and Transwell assays were employed to monitor cell migration and invasion, while protein expression was determined using western blotting. Results: The results showed that ACC was significantly enhanced in SNU-1 gastric cancer cells (4.2- fold). Silencing of ACC in SNU-1 gastric cancer cells caused significant decrease in cell proliferation (p < 0.05). Electron microscopy examination showed that ACC silencing triggered autophagic cell death in SNU-1 cells, and increased expression of LC3 II. Results from DAPI and AO/EB assays demonstrated that ACC silencing also promoted apoptosis in SNU-1 gastric cancer cells. Annexin V/PI assay results revealed that apoptotic cell population increased from 2.7 to 13.8 % due to ACC silencing (p < 0.05). Moreover, Bax expression increased, while Bcl-2 expression decreased upon ACC silencing. Transwell assay results indicate that ACC silencing caused marked decrease in the invasion of the SNU-1 cells and downregulation of the expressions of MMP-2 and MMP-9 (p < 0.05). Conclusion: ACC is likely to be an important therapeutic target for gastric cancer.

scholarly journals Inactivation of Akt by arsenic trioxide induces cell death via mitochondrial-mediated apoptotic signaling in SGC-7901 human gastric cancer cells

2014 ◽  
Vol 31 (4) ◽  
pp. 1645-1652 ◽  
Author(s):  
YAN-HUI GAO ◽  
HAO-PENG ZHANG ◽  
SHU-MENG YANG ◽  
YUE YANG ◽  
YU-YAN MA ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Apoptotic Signaling

scholarly journals Suppression of transient receptor potential melastatin 7 channel induces cell death in gastric cancer

2008 ◽  
Vol 99 (12) ◽  
pp. 2502-2509 ◽  
Author(s):  
Byung Joo Kim ◽  
Eun Jung Park ◽  
Jae Hwa Lee ◽  
Ju-Hong Jeon ◽  
Seon Jeong Kim ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Melastatin ◽  
Transient Receptor

Akebia saponin PA induces autophagic and apoptotic cell death in AGS human gastric cancer cells

2013 ◽  
Vol 59 ◽  
pp. 703-708 ◽  
Author(s):  
Mei-Ying Xu ◽  
Dong Hwa Lee ◽  
Eun Ji Joo ◽  
Kun Ho Son ◽  
Yeong Shik Kim
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells
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